PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16166335-6 2005 Furthermore, cells that were pretreated with 100 nmol/L 12-O-tetradecanoyl phorbol-13-acetate, and then treated with 25 micromol/L PEITC-NAC, underwent enhanced apoptosis compared with cells that were treated with PEITC-NAC alone; cells treated with 12-O-tetradecanoyl phorbol-13-acetate alone showed active cell growth without apoptosis. Tetradecanoylphorbol Acetate 56-93 X-linked Kx blood group Homo sapiens 137-140 25310083-1 2014 In the present study, in order to clarify the preventive mechanism of N-acetyl-L-cysteine (NAC) on arsenite-induced apoptosis in U937 cells, which lack functional p53, the cytotoxicity among U937 cells [monocytes and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated macrophages] receiving NAC treatment at different times post arsenite treatment was examined. Tetradecanoylphorbol Acetate 217-253 X-linked Kx blood group Homo sapiens 91-94 25310083-1 2014 In the present study, in order to clarify the preventive mechanism of N-acetyl-L-cysteine (NAC) on arsenite-induced apoptosis in U937 cells, which lack functional p53, the cytotoxicity among U937 cells [monocytes and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated macrophages] receiving NAC treatment at different times post arsenite treatment was examined. Tetradecanoylphorbol Acetate 255-258 X-linked Kx blood group Homo sapiens 91-94 27011169-5 2016 Our results showed significantly accelerated biodegradation of ox-SWCNTs and OH-SWCNTs in macrophages activated by phorbol myristate acetate (PMA), which could be prevented by N-acetyl-l-cysteine (NAC), whereas p-SWCNTs were resistant to biodegradation. Tetradecanoylphorbol Acetate 115-140 X-linked Kx blood group Homo sapiens 197-200 27011169-5 2016 Our results showed significantly accelerated biodegradation of ox-SWCNTs and OH-SWCNTs in macrophages activated by phorbol myristate acetate (PMA), which could be prevented by N-acetyl-l-cysteine (NAC), whereas p-SWCNTs were resistant to biodegradation. Tetradecanoylphorbol Acetate 142-145 X-linked Kx blood group Homo sapiens 197-200 17131377-6 2007 Interestingly, ICAM-1 expression in response to TPA-induced PKC activation was linked to the generation of reactive oxygen species (ROS), as pretreatment with NAC (an ROS scavenger) blocked both ErK1/2 activation and ICAM-1 expression induced by TPA. Tetradecanoylphorbol Acetate 48-51 X-linked Kx blood group Homo sapiens 159-162 17131377-6 2007 Interestingly, ICAM-1 expression in response to TPA-induced PKC activation was linked to the generation of reactive oxygen species (ROS), as pretreatment with NAC (an ROS scavenger) blocked both ErK1/2 activation and ICAM-1 expression induced by TPA. Tetradecanoylphorbol Acetate 246-249 X-linked Kx blood group Homo sapiens 159-162 16945329-4 2006 PPARgamma expression in response to TPA was attenuated by pretreatment with bisindolylmaleimide I, N-acetyl-L-cysteine (NAC) and PD98059. Tetradecanoylphorbol Acetate 36-39 X-linked Kx blood group Homo sapiens 120-123 16945329-6 2006 Pretreatment with bisindolylmaleimide I or NAC blocked TPA-induced phosphorylation of extracellular signal-regulated kinase (ERK), suggesting that ERK-mediated signaling is also involved in the induction of PPARgamma. Tetradecanoylphorbol Acetate 55-58 X-linked Kx blood group Homo sapiens 43-46 16166335-6 2005 Furthermore, cells that were pretreated with 100 nmol/L 12-O-tetradecanoyl phorbol-13-acetate, and then treated with 25 micromol/L PEITC-NAC, underwent enhanced apoptosis compared with cells that were treated with PEITC-NAC alone; cells treated with 12-O-tetradecanoyl phorbol-13-acetate alone showed active cell growth without apoptosis. Tetradecanoylphorbol Acetate 56-93 X-linked Kx blood group Homo sapiens 220-223 16166335-6 2005 Furthermore, cells that were pretreated with 100 nmol/L 12-O-tetradecanoyl phorbol-13-acetate, and then treated with 25 micromol/L PEITC-NAC, underwent enhanced apoptosis compared with cells that were treated with PEITC-NAC alone; cells treated with 12-O-tetradecanoyl phorbol-13-acetate alone showed active cell growth without apoptosis. Tetradecanoylphorbol Acetate 250-287 X-linked Kx blood group Homo sapiens 137-140 10708546-3 2000 Cystathionine ketimine and NAc-OCPC also enhanced superoxide generation induced by opsonized zymosan (OZ) but not that induced by arachidonic acid (AA) and phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 189-192 X-linked Kx blood group Homo sapiens 27-30 12404881-5 2002 At concentrations of 16 and 35 mumol/l, NAC significantly reduced in a concentration-dependent manner the activation of polymorphonuclear neutrophils (PMNs) oxidative bursts induced by all of the stimulants (C. albicans, formyl-methionyl-leucyl-phenylalanine (fMLP), phorbol myristate acetate (PMA)). Tetradecanoylphorbol Acetate 267-292 X-linked Kx blood group Homo sapiens 40-43 12404881-5 2002 At concentrations of 16 and 35 mumol/l, NAC significantly reduced in a concentration-dependent manner the activation of polymorphonuclear neutrophils (PMNs) oxidative bursts induced by all of the stimulants (C. albicans, formyl-methionyl-leucyl-phenylalanine (fMLP), phorbol myristate acetate (PMA)). Tetradecanoylphorbol Acetate 294-297 X-linked Kx blood group Homo sapiens 40-43 11299737-4 2001 NAC inhibited TPA-enhanced invasion dose-dependently. Tetradecanoylphorbol Acetate 14-17 X-linked Kx blood group Homo sapiens 0-3 11299737-5 2001 TPA increased the MMP-9 production by T24 cells without altering expression of TIMP-1 gene, while NAC suppressed TPA-enhanced production of MMP-9. Tetradecanoylphorbol Acetate 113-116 X-linked Kx blood group Homo sapiens 98-101 2112750-1 1990 We show that the stimulation of human immunodeficiency virus (HIV) brought about by tumor necrosis factor alpha and phorbol 12-myristate 13-acetate can be inhibited by adding N-acetyl-L-cysteine (NAC). Tetradecanoylphorbol Acetate 116-147 X-linked Kx blood group Homo sapiens 196-199 9350434-2 1997 Since these latter compounds were known to activate NF-kappa B translocation in a redox-sensitive way, we have demonstrated that NF-kappa B activation by PMA was resistant to antioxidant N-acetyl-L-cysteine (NAC) and sensitive to kinase inhibitors staurosporine and H7 while activation by H2O2 or TNF-alpha were not. Tetradecanoylphorbol Acetate 154-157 X-linked Kx blood group Homo sapiens 208-211 9277499-3 1997 Monocytic cell adhesion to EC in response to tumor necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS), alpha-thrombin, or phorbol 12-myristate 13-acetate (PMA) was similarly inhibited by NAC. Tetradecanoylphorbol Acetate 131-162 X-linked Kx blood group Homo sapiens 196-199 8194136-3 1994 We confirmed that N-acetyl-L-cysteine (NAC), a cysteine prodrug which maintains intracellular GSH levels during oxidative stress, inhibits in the chronically infected U1 cells, the stimulation of HIV replication induced by phorbol 12-myristate 13-acetate (PMA), interleukin-6 (IL-6) or granulocyte-macrophage colony stimulating factor (GM-CSF). Tetradecanoylphorbol Acetate 223-254 X-linked Kx blood group Homo sapiens 39-42 31285782-10 2019 Interestingly, treatment with either N-acetyl-L-cysteine (NAC) or diphenyleneiodonium (DPI) reduced the PMA-stimulated phosphorylation of these PTKs, implicating a potential role in cellular ROS signaling. Tetradecanoylphorbol Acetate 104-107 X-linked Kx blood group Homo sapiens 58-61